The relationship between distribution of blood volume in the capacity space and plasma renin levels will be investigated in patients and control subjects. We will test the hypothesis that the "effective" volume related to renin levels is the cardiopulmonary blood volume, presumably through the effect of this volume on cardiopulmonary mechanoreceptors. We observed that patients with low-renin hypertension have a normal total blood volume but maintain a larger cardiopulmonary volume. The low renin in these patients may stem from suppression of renal sympathetic tone by volume-stimulated cardiopulmonary receptors. In this investigation, patient's renin status will be classified on various states of sodium balance. Using negative pressure to the legs, the cardiopulmonary blood volume in hypertensives will be decreased to normal and renin response analyzed. Influences of sodium depletion on cardiopulmonary volume and renin will be studied. In controls and patients the functional relationship between the right atrial pressure-cardiopulmonary volume and renin-sympathetic responses will be investigated by stepwise decrease of atrial pressure (tilt, negative leg pressure) and observation of reflex (heart rate, peripheral resistance, forearm flow) and humoral (renin, catecholamines) responses. This investigation may elucidate mechanisms of renin suppression in some patients with low-renin hypertension and may define the contribution of volume factors to overall physiologic control of plasma renin in human beings.